Latest Coronavirus News
By Dennis Thompson HealthDay Reporter
WEDNESDAY, June 30, 2021
Two-thirds of a group of 30 COVID long-haul patients had high levels of Epstein-Barr antibodies, suggesting that EBV lying dormant in their bodies had been reactivated by their coronavirus infection, researchers reported.
“While SARS-CoV-2 clearly causes acute COVID-19 disease, the inflammatory consequences of this may lead to the participation of other agents, specifically EBV, in the complex pathogenesis of the disease-associated problems over the long-term,” said lead researcher Jeffrey Gold, president of World Organization, an environmental nonprofit group.
More than 95% of adults carry Epstein-Barr, which is a herpesvirus, the researchers said in background notes. The virus is the most common cause of mononucleosis, a disease that also leaves its sufferers persistently exhausted.
“It’s just there. It remains latent in yourself, and anything that stresses your body can cause it,” said Dr. Amesh Adalja, a senior scholar with the Johns Hopkins Center for Health Security in Baltimore. “If you look at EBV viral loads in ICU patients, they’re going to be elevated. Anybody in any kind of stressful situation, there’s a likelihood that [Epstein-Barr] would be reactivated or it would be replicating.”
However, Adalja added that more evidence is needed to prove the connection, given that EBV is widespread among humans and can be triggered by physical or psychological stress.
For this study, Gold and his colleagues surveyed 185 COVID patients and found that about 30% were suffering long-haul symptoms.
Taking a closer look at 30 of the long-haul COVID patients, researchers found that 20 of them carried levels of EBV antibodies high enough to suggest Epstein-Barr reactivation.
These long-haul patients with high EBV antibody levels reported fatigue, insomnia, headaches, body aches and confusion as their most common symptoms. Other symptoms included tinnitus (ringing in the ears), hearing loss and skin rashes.
The researchers argued that COVID infection is causing EBV to flare in some patients, and that is what triggers their long-haul symptoms.
“The coronavirus that leads to COVID-19 disease induces significant local and systemic activation of inflammatory cascades,” explained study co-author David Hurley, a professor and molecular microbiologist at the University of Georgia. “Either local or systemic inflammatory activation is known to reactivate herpesviruses that have gone latent, and EBV in particular is strongly reactivated from immune and epithelial tissues by inflammatory triggers.”
More studies with larger pools of patients are needed before this will be anything beyond a hypothesis, Adalja said.
“This is really not anything that I would think is definitive at this point. There are a lot more details to study,” he noted.
The study doesn’t provide strong evidence to argue that these patients were suffering an Epstein-Barr reactivation powerful enough to be the source of long-haul symptoms, Adalja said.
“They didn’t really prove that because they’re looking at antibodies,” Adalja said. “They don’t really do much with viral loads, and the couple of viral loads they report are in the hundreds, not really high.”
If it eventually proves true, this could offer doctors new ways to help people with long-haul COVID, Hurley said.
“Screening for EBV reactivation early in the process would offer the physician an opportunity to utilize a number of drugs designed to limit herpesvirus load in patients and minimize the extent and duration of the long COVID condition,” Hurley said. “Most patients could benefit from relatively low-cost screening, even if it just means that no evidence of EBV reactivation is seen. EBV can be monitored with simple, relatively low-cost serum tests.”
The new study was published recently in the journal Pathogens.
SOURCES: Jeffrey Gold, president, World Organization, Watkinsville, Ga.; Amesh Adalja, MD, senior scholar, Johns Hopkins Center for Health Security, Baltimore; David Hurley, PhD, professor and molecular microbiologist, University of Georgia; Pathogens, June 17, 2021
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